The Role of <i>Megalobrama amblycephala bcl2l13</i> Gene in Apoptosis and Autophagy

The Role of <i>Megalobrama amblycephala bcl2l13</i> Gene in Apoptosis and Autophagy

Bcl-2-like protein 13 (Bcl2l13) plays an important role in the cell apoptosis and mitochondrial autophagy of mammals. However, the role of <i>bcl2l13</i> remains unclear in fish. Therefore, in this study, the function of <i>Megalobrama amblycephala bcl2l13</i> gene in apoptos...

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Bibliographic Details
Main Authors: Suzhen Wang, Xuanhui Li, Danyang Wu, Zexia Gao, Hong Liu, Huanling Wang
Format: Article
Language:English
Published: MDPI AG 2025-05-01
Series:Fishes
Subjects:
<i>bcl2l13</i>
fish
apoptosis
autophagy
Online Access:https://www.mdpi.com/2410-3888/10/6/247
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Summary:Bcl-2-like protein 13 (Bcl2l13) plays an important role in the cell apoptosis and mitochondrial autophagy of mammals. However, the role of <i>bcl2l13</i> remains unclear in fish. Therefore, in this study, the function of <i>Megalobrama amblycephala bcl2l13</i> gene in apoptosis and autophagy was investigated. The results showed that the overexpression of <i>M. amblycephala bcl2l13</i> under hypoxic condition led to a reduction of reactive oxygen species (ROS), an increase in the expression levels of autophagy-related genes (<i>p62</i>, <i>lc3</i>, <i>pink1</i>), and a disruption of mitochondrial structure. However, deleting its transmembrane (TM) and Bcl-2 homology no (BHNo) domains decreased the P62 protein level, suggesting its essential role in autophagy. Furthermore, <i>bcl2l13</i> overexpression inhibited cell proliferation and increased apoptosis. Additional studies revealed that the permeability of the mitochondrial permeability transition pore (mPTP) increased after overexpression of <i>bcl2l13</i>, but decreased upon deletion of the TM domain. Additionally, hypoxia led to elevated Bcl2l13 and P62 levels, and caused mitochondrial damage in <i>M. amblycephala</i> liver after 48 h of treatment. In conclusion, <i>bcl2l13</i> may induce autophagy, inhibit cell proliferation and promote apoptosis, while its TM and BHNo domains play pivotal roles in these processes.
ISSN:2410-3888

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